ICTS

TBA

TBA

In nature, organisms evolve to best fit their ecological niches, and while doing so, arrange themselves into discrete, reproductively isolated groups called species. While the evolutionary response of an organism is shaped by adaptive mutations, random genetic drift, and bottlenecks, the fundamental forces driving speciation events are largely unknown. In fact, speciation is, at times, characterized to be simply a by-product of an adaptive process. However, the reasons why an adaptive process defined by interaction between a genome and an environment, should dictate a process which is defined by interaction of two distinct genomes are not clear. While a number of theoretical and conceptual ideas and models have been proposed to explain speciation, no model systems or systematic experimental characterization of speciation events exists. This lack of understanding of speciation events forms the basis of our work. In this context, a study of factors that contribute to the process of speciation is of interest to us. Towards this end, we use Saccharomyces cerevisiae and the melibiose utilization system as the model system to study dynamics of speciation in allopatry and sympatry.

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My current research focuses on tracing the ancestral origin and biogeographical affiliation of various human and endangered animal populations and deducing Ancestry Informative Markers (AIMs) for the same. There is an eternal quest to uncover our roots and our ancestral
origin to answer the primal questions ‘who am I?’ and ‘where am I from?’. Our DNA determines not only who we are but holds the key to uncovering our true ancestral past. A plethora of information stored inside the genome reflects our uniqueness and proximity to
different ancestral and modern-day populations. Given high correspondence between our genetic make-up and the geographical origin of our forefathers, it is possible to glean into precise ancestral origin using the genetic information. While genetically all humans are >99% identical, there are variations in our DNA that makes us unique. The most common type of variation is a single base pair change in the DNA known as Single Nucleotide Polymorphisms (SNPs). A collection of SNPs, commonly known as Ancestry Informative
Markers (AIMs), exhibit large differences among ancestral populations. These AIMs panels can help in tracing one’s ancestry with high precision. Understanding our ancestry is not only a ‘homing’ tool bringing you closer to your evolutionary past but also holds the key to detect ancestry specific disorders, develop ancestry-specific medicine and identify potential suspects by shortlisting individuals based on their ancestry. Further, the knowledge of ancestry can greatly aid in the preservation of biological diversity by maximizing genetic diversity through outbreeding and genomic admixture and preventing inbreeding among genetically related individuals. Thus determination of ancestry and AIMs can be monumental in the conservation of endangered wild animals.

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Technological advances in sequencing have propelled ancient DNA research into the ‘paleogenomics’ era, accompanied by a tremendous increase in the amount of generated data. Additionally, continued efforts towards optimizing laboratory pipelines, including sampling, DNA extraction, and library preparation techniques, have resulted in increased DNA yield from ancient samples. These genome-wide datasets are being used to reconstruct past population structures and understand how processes such as ancient migrations, admixture, selection, environmental changes, and epidemics have shaped present-day human gene pools. My talk will focus on the contributions of ancient DNA research to the emerging picture of modern human dispersals and provide perspectives on how collaborative efforts with the fields of archaeology and anthropology are providing a new dimension to our understanding of the human past.

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TBA

How do new species arise? This is one of the fundamental problems of evolutionary biology. Although considerable effort has been devoted to understanding the underlying mechanisms of speciation, it is far from complete. Speciation in eukaryotes is due to reproductive isolation (i.e., pre-zygotic or post-zygotic) and mechanisms of post-zygotic reproductive isolation are better understood than that of pre-zygotic isolation. Dobzhansky-Muller incompatibilities represent a major driver of post-zygotic reproductive isolation between species. They are caused by two or more interacting components that cannot function properly when mixed with alleles from different species. At incipient stages of speciation, complex incompatibilities involving multiple genetic loci with weak effects are frequently observed, but their underlying mechanism remains elusive. We observed perturbed proteostasis manifesting as proteotoxic stress in introgressed hybrids of the yeast Saccharomyces cerevisiae carrying one or two chromosomes from its close relative Saccharomyces bayanus. Proteotoxicity in these introgressed yeast hybrids caused compromised fitness (mitosis) and sporulation (meiosis). The level of proteotoxicity was correlated with the number of multi-protein complexes encoded on replaced chromosomes and could be alleviated or aggravated by up- or down-regulating ubiquitin-proteasome degradation machinery. Using proteomic approaches, we detected destabilized multi-protein complexes in introgressed hybrids, providing evidence that proteotoxicity is due to improper interactions between the complex-subunits encoded by different genomes. Our results reveal the general role played by impaired protein complex assembly in complex incompatibilities.

This lecture will begin with a historical overview of thinking and mathematical modelling of adaptation (Fisher, Kimura, Maynard Smith). We will then derive some basic results from Fisher’s
Geometric Model and discuss their implications. Finally, we will give an overview of the three regimes of adaptation: the single sweep, clonal interference and multiple mutation regimes.

Suggested reading: Orr 2005, Tenaillon 2014 (pp 1-8)

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Morphologically complex polymorphisms may be governed by simple genetic principles. Novel adaptive mutations that are genetically dominant over wild-type are able to rapidly advance through populations under strong selection (Haldane’s sieve). Supergene-like architecture should protect these mutations responsible for ecological morphs that occupy distinct adaptive peaks, but occasional recombination may fuel diversification of adaptive phenotypes. We demonstrate these principles in the female-limited, polymorphic Batesian mimicry in Papilio polytes. This polymorphic mimicry is complex but we found that it was fully governed in all mimetic forms by allelic variation of doublesex, a single switch-locus. Phylogenetic analysis revealed that the evolution of novel mimetic forms followed Haldane’s sieve, the most recently evolved mimetic form being universally dominant. The supergene-like genetic architecture of mimetic polymorphism was attributed to a large inversion around doublesex, but mimetic female forms shared the precise breakpoints of the inversion. Surprisingly, phenotypic intermediates due to recombination within this inversion were exceedingly rare. However, recombinations between exon 1 of the universally dominant female form and remaining exons of a recessive female form produced a novel, stable intermediate phenotype combining wing patterns of different mimetic forms, which is highly unusual for Batesian mimetic wing patterns with complete dominance. We thus show how an interaction of Haldane’s sieve, a strong genetic architecture and recombination may stabilize balanced polymorphisms but simultaneously facilitate the evolution novel forms.​

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